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FEMS Microbiol Rev. 2014 Nov;38(6):1172-201. doi: 10.1111/1574-6976.12083. Epub 2014 Sep 26.

The bacterial translation stress response.

Author information

1
Gene Center, Department for Biochemistry, Ludwig-Maximilians-Universität München, Munich, Germany; Center for integrated Protein Science Munich (CiPSM), Ludwig-Maximilians-Universität München, Munich, Germany.

Abstract

Throughout their life, bacteria need to sense and respond to environmental stress. Thus, such stress responses can require dramatic cellular reprogramming, both at the transcriptional as well as the translational level. This review focuses on the protein factors that interact with the bacterial translational apparatus to respond to and cope with different types of environmental stress. For example, the stringent factor RelA interacts with the ribosome to generate ppGpp under nutrient deprivation, whereas a variety of factors have been identified that bind to the ribosome under unfavorable growth conditions to shut-down (RelE, pY, RMF, HPF and EttA) or re-program (MazF, EF4 and BipA) translation. Additional factors have been identified that rescue ribosomes stalled due to stress-induced mRNA truncation (tmRNA, ArfA, ArfB), translation of unfavorable protein sequences (EF-P), heat shock-induced subunit dissociation (Hsp15), or antibiotic inhibition (TetM, FusB). Understanding the mechanism of how the bacterial cell responds to stress will not only provide fundamental insight into translation regulation, but will also be an important step to identifying new targets for the development of novel antimicrobial agents.

KEYWORDS:

antibiotic stress; mRNA truncation; nutrient depletion; stationary phase; toxin-antitoxin modules; translational stalling

PMID:
25135187
PMCID:
PMC4227928
DOI:
10.1111/1574-6976.12083
[Indexed for MEDLINE]
Free PMC Article

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